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COMPLETE Pathophysiology Notes - Part 3 (4.0ed the final exam!)

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Boston College
NURS 2080

Pathophysiology Exam 3 SG FLUID & ELECTROLYTE IMBALANCES Body Fluid Distribution Intracellular 2/3 of body water is within our cells Extracellular (interstitial, intravascular, Transcellular) Fluid transportation within body is important Intravascular Plasma/serum Fluid can be pulled from extracellular space when needed to help with blood pressure Transcellular Fluid in pericardial sac, pleural cavity, peritoneum, sweat, urine, lymph system, etc Intracellular and extracellular fluid distribution ICF & ECF rely on concentration of sodium Osmolality – 275-295 mOsm/kg Where sodium goes, water follows (osmolality, osmolarity = synonyms) <275 = low osmolality (solution low in solutes – dilute) >295 = excess solutes (high concentration solution) Osmotic activity of serum (plasma) Determined by concentration of Na+ Tonicity Hypotonic – H2O osmotically pulled into cell, swelling Hypertonic – cell shrinks as water is pulled out of cell Isotonic – neither shrink nor swell Mechanisms of H20 & Na+ Regulation Low & high circulating volumes results in feedback mechanisms Low (hypotensive, fluid lost), body conserves H2O and Na+ Kidneys conserve Na+; water follows High (have more fluid than body needs) Kidneys excrete sodium; water follows Stimulation of osmoreceptors Causes thirst Located near hypothalamus, they sense osmolality of blood If [solutes] too high (patient dehydrated), ADH and thirst mechanism activated Baroreceptors Located in atria, in large pulmonary vessels, in aortic arch They sense low or high circulating volume (by stretch of vessels near heart) Stimulate sympathetic response if low volume Increases HR and blood flow to kidney GFR goes up due to rise in BP Stimulate ADH release if low volume Heart Atria Release ANP if overstretched Ventricles Release BNP if overstretched ANP & BNP Both cause kidneys to excrete sodium, water follows Kidneys – if low blood flow Sympathetic response RAAS – renin-angiotensin-aldosterone system Increases HR and release of aldosterone Assessment of Water Balance Metabolic rate Healthy persons require 100ml of H2O per 100 calories metabolized for dissolving & eliminating metabolic waste Example: 1800 calories requires 1800ml of H2O We need 1800 ml fluid to help process our metabolic functions Body normally requires 2-2.5 liters fluid (includes liquid content within solids) With fever, metabolic rate rises approximately 7% for every 1 degree F Fever increases metabolic rate (we lose fluid and need to catch up to put more in body) Increased metabolic rate = fluid loss from RR and sweating Increases respiratory rate causing additional loss of water vapor through the lung Output: sweat, urination (loss of 1500ml per day), 200 ml within feces, fluid lost in lungs Oxidative metabolism = a chemical process in which oxygen is used to make energy from carbohydrates. Also known as aerobic respiration, cell respiration, or aerobic metabolism (amount of water gained from these processes varies from 150-300mL/day, depending on metabolic rate). Isotonic fluid volume deficit Decrease in ECF with proportionate losses of Na & H2O (We lose equal amounts of sodium and water) Causes: loss of body fluids & decreased intake GI – vomiting & diarrhea, NG tubes, fistulas Fistulas = abnormal openings (can go from bowel to skin in GI tract) Urine – diuretics, hyperglycemia Hyperglycemia leads to osmotic pulls; puts more fluid in vascular space, polyuria from elevated glucose levels Skin – sweating (fever or exercise) We lose up to 3L of fluid per day with fever Can lose 2L from exercise on a hot day Endocrine (low aldosterone  Na lost in urine) Third space – ECF sequesters in serous cavities Ascites = fluid goes in peritoneal cavity instead of staying within vascular space Isotonic Volume Overload (sodium and water excess, in equal amounts) Isotonic expansion of ECF compartment Includes interstitial & vascular volumes Results via Na excess with proportionate H2O Causes – disorders related to Na & H2O elimination Heart Failure (inability to pump out into periphery) BP not high enough, aldosterone released, sodium/water retained This causes excess fluid volume Renal Failure Body can’t get rid of excess fluid through kidneys; it’s retained Liver Failure Issue with aldosterone Fluid retention Fluid can sequester in abdomen Excess overall fluid Corticosteroid Excess Meds; tend to increase sodium reabsorption by kidneys Circulatory Overload Increase in blood volume & ECF Can happen when patient given too many IV fluids Manifestations of Isotonic volume issues (*Important*) In decreased interstitial fluid volume, dry membranes occurs because fluid is being sucked into vascular space to help maintain homeostasis In decreased vascular volume, postural hypotension occurs (when you sit or stand up, drop in BP) Hypovolemic shock In excess Might see JVD Pulmonary – crackles If severe enough, pink frothy sputum (pulmonary edema) Hematocrit level rises with dehydration because loss of body water. (Hematocrit = ratio of RBCs to total blood volume) Causes of Edema Increased Capillary Filtration Pressure Increased arterial pressure Dependent edema (in ankles from standing) Increased resistance to outflow – venous obstruction Thrombophlebitis DVT Capillary distension Increased vascular volume (congestive heart failure, kidney disease) Fluid in capillary bed being pushed out to interstitial space Kidney disease: increased hydrostatic pressure; can’t urinate, fluid stays in body Decreased capillary colloidal osmotic pressure Inadequate production or loss of proteins (albumin) Proteins important in maintaining osmotic pressure Any fluid getting pulled out is pulled back in when we have good colloidal pressure Body loses ability to pull fluid back into vessel Liver failure, malnutrition, extensive burns Liver important in maintaining proteins Causes generalized edema Increased capillary permeability Capillary pores enlarge, protein leak interstitially Allergic reactions, inflammation **Increased hydrostatic pressure** Obstruction of lymphatic flow Lymphs are backup when fluid leaks out and proteins can’t pull it back in Lymph system absorbs fluid in normal person Decreased ability to pull in extra fluid (lymph system absorbs fluid in normal person) Lymphedema Cancer, lymph node removal, trauma, infection Types of edema Peripheral edema Assessed by visual inspection or daily weight Transcellular edema Lymphedema has honeycomb appearance; regular edema does not Electrolyte table (don’t have to memorize numbers) Electrolyte Extracellular Intracellular Sodium 135-145 mEq/L 10-14 mEq/L Potassium (28 times more 3.5-5.0 mEq/L 140-150 mEq/L concentrated inside cell than outside) Chloride 98-106 mEq/L 3-4 mEq/L Bicarbonate 24-31 mEq/L 7-10 mEq/L Calcium 8.5-10.5 mg/dL < 1mg/dL Phosphorus 2.5-4.5 mg/dL 4 Magnesium 1.8-3.0 mg/dL variable Electrolytes are substances that dissociate in solution to form charged particles called ions. Cations are + charged ions All body fluids contain equal amounts of anions & cations Because of attraction forces, + ions are always accompanied by - charged ions Ions may be exchanged + ion for another + ion; - ion for another - ion Glucose and urea are particles that do not contain charges Interstitial fluid & plasma basically contain the same electrolyte composition but plasma contains a large amount of proteins Intracellular electrolyte composition is quite different from extracellular, but # of charges (cations & anions) are basically equal between the 2 compartments Remember: proportionate changes in H20 volumeF osmolarity; changes in Na are usually accompanied by Sodium (Na+) Major cation of ECF Anions are Cl & HCO3 Regulated by: Kidneys Aldosterone (secreted when) Na levels are depressed K levels are increased Renal perfusion is decreased Natriuretic peptides (ANP, BNP) Necessary for body functions Too much sodium intake ruins heart Hyponatremia Types Hypotonic/hypervolemic Increased vascular volume (water retention)  dilutes sodium Loss of salt and water in fluid loss Excessive sweating, GI losses, SIADH, heart failure Hypertonic Osmotic shift from ICF to ECF Hyperglycemia Reabsorption of water drawn by glucose Manifestations Swelling (water retention; water sucked back into intracellular space) This effects depolarization Muscle cramps, motor weakness, W&F, headache Seizures if sodium is low enough Edema to brain tissue Hypernatremia Hypertonicity of ECF & intracellular dehydration Hypertonicity = high osmolality (body holds onto fluids) Cells shrink Osmolality elevated; cells bumping into each other More sodium in serum – it wants equilibrium so pulls water out of cells into serum to help balance Causes Watery diarrhea Strenuous exercise Water lost through urine Disproportionate loss of body H2O in relation to Na At risk individuals Those who cannot sense thirst or have no access to water Elderly (decreased thirst sensation) Infants Trauma/head injury patients Manifestations Thirst = early symptom Low urine output Dry mucous membranes (water pulled from interstitial space) CNS symptoms – irritability, restlessness, headache Seizures and comas Potassium – major cation of ICF Maintains intracellular osmolality Regulates resting membrane potential Opens the Na+ channels during action potential Regulates rate of membrane repolarization Maintains acid–base balance Catalyst to transform carbohydrates into energy Converts glucose into glycogen Convert amino acids into proteins CRITICAL in conduction of nerve impulses & muscle excitability Mechanisms of potassium regulation Renal regulation Kidney is major route of K elimination Aldosterone Regulates K elimination in distal tubule (aldosterone lowers K levels) K/hydrogen ion exchange mechanism (in collecting duct of kidney) K is high Excreted in the urine & hydrogen is pulled back into the blood This can cause metabolic acidosis K is low K is reabsorbed from the urine & hydrogen is excreted into the urine. Leads to metabolic alkalosis Transcellular buffer system - redistributes between ECF & ICF Removes K+ from or releases K into serum as needed K temporarily shifted into RBCs, muscle, liver & bone 1. When BP is low: aldosterone excreted to help increase BP (vasoconstrictor & Na increase) 2. Feedback regulation - When K is high: adrenal cortex will secrete aldosterone to lower K levels Hypokalemia Causes Inadequate intake Excessive vomiting Signs and symptoms Neuro = weakness, fatigue (think of SLOWING with hypokalemia) CV = EKG changes GI = slowing of smooth muscle, not effectively pumping intestines, causes nausea and vomiting GU = polyuria (kidney holds onto K to improve levels in blood – this causes sodium to leave in distal tubule) Hyperkalemia Mild hyperkalemia causes a peak T wave related to rapid repolarization Causes Renal failure Manifestations Neuro – mild muscle weakness, mild paresthesia (tingling, pricking, burning sensation) CV - EKG changes, Peaked T waves (mild) Prolonged PR interval Widened QRS Lethal arrhythmias Cardiac arrest R – dyspnea (muscle weakness) GI – diarrhea, cramps (mild) Cramps from increased excitability of muscles Muscle weakness (severe) Prolongs PR intervals  delayed depolarization of atria (end up with Brady arrhythmias – slow HR and conduction problems) Hyperkalemia  delayed depolarization but rapid repolarization Blood K+ levels control resting potential Decreased K lowers resting potential away from threshold  cells fire less easily  mild hypokalemia symptoms (*Severe hypokalemia differs*) In hyperkalemia, resting membrane close to threshold Cells can’t d/repolarize (meaning the next action potential will not occur) Hyperkalemia causes kidney disorders Calcium 99% bones, <1% ICF, 0.1 - 0.2% ECF ECF – 3 forms Protein bound mostly to albumin Complexed Ionized – moves between vessels & cells as needed (free calcium) Takes part in intracellular activities Membrane potentials (stabilizing cell membrane, blocks Na transport into cell) Creates excitability of tissues Neuronal excitability Necessary for muscle contraction Essential for blood clotting Regulation – PTH Stimulated by low calcium levels Activated by high phosphorus levels We take in calcium thru GI tract and can store in bones Taken from bones in times of need With mild to moderate hyperkalemia, there is reduction of the size of the P wave and development of peaked T waves. Severe hyperkalemia results in a widening of the QRS complex. There appears to be a direct effect of elevated potassium on some of the potassium channels that increases their activity and speeds membrane repolarization. Also, hyperkalemia causes an overall membrane depolarization that inactivates many sodium channels. The faster repolarization of the cardiac action potentials causes the tenting of the T waves, and the inactivation of sodium channels causes a sluggish conduction of the electrical wave around the heart, which leads to smaller P waves and widening of the QRS complex. Regulation by PTH Hypocalcemia Causes Milk products not ingested – can be related to nutritional deficiencies (calcium is also in dark green leafy vegetables) Manifestations – increased excitability, repetitive responses to one stimulus Neuro – paresthesia, muscle spasms, tetany, hyperactive reflexes CV – hypotension, HF, long QT, cardiac arrhythmias Hyperactive reflexes Calcium channels important in heart muscle activity Skeletal - fractures (chronic) Bones are brittle Numbing/tingling around lips Assessment Tapping on facial nerve, notice spasm Seen in patients with removed thyroid Hypercalcemia Causes Malignancy (can cause substances that break down bown) Manifestations – decreased neural excitability & muscle function Neuro – lethargic, behavioral changes, coma CV – HTN, increased contractility, arrhythmias GI – N/V, constipation GU – high output (constantly filtering out thru urine), renal calculi (calcium stones) Calcium maintained by ambulating and moving around Low extracellular calcium will slightly depolarize the cells such that they have a reduced firing threshold, giving rise to hyperexcitability. ACID-BASE Terminology Disassociate – separation of a molecule into two or more simpler fragments Carbonic Anhydrase (CA) – enzyme found in all RBC & renal tubular cells Responsible for the rapid conversion of CO2 and H2O into carbonic acid Also helps carbonic acid to disassociate into CO2, H2O (Hydration reaction of CO2 is generally very slow, but carbonic anhydrase increases rate of conversion) CA found in RBCs, renal tubular cells, and other tissues of body Carbonic Acid (H2CO3) – CO2 dissolved in water Bicarbonate – base; main base in body Acids Molecules that can dissociate & release H ion Example: HCl dissociates in water to form H+ and Cl- ions Byproduct of a metabolic process Volatile (easily vaporized) Carbonic acid (H2CO3) is in equilibrium with CO2 Eliminated by lungs Non-volatile Occurs from metabolism of dietary proteins, CHO, & fats Oxidation produces HCl, sulfuric acid, and phosphoric acid Incomplete oxidation Glucose results in lactic acid Fats produce ketoacids Eliminated by kidneys after being buffered Bases Base – ion or molecule that can accept a H+ ion Example: HCO3- can accept a H+ to form H2CO3 Sources of bases Metabolism of amino acids (aspartate, glutamate) Metabolism of organic anions (citrate, lactate, acetate) Carbon dioxide transport CO2 is an end product of aerobic metabolism Diffuses and transported in circulation as either a dissolved gas, bicarbonate or carbaminohemoglobin 1. Dissolved gas When there is excess of CO2 in the plasma it moves to the RBCs 2. HCO3 is made through the following steps CO2 moves into RBC & meets with carbonic anhydrase within RBC it is allowed to bind with H20 to form carbonic acid Dissociation of H2CO3 occurs next & the acid is split into H+ & HCO3- HCO3- diffuses into plasma and is now allowed to participate in acid base regulation This diffusion occurs when RBC exchanges HCO3- for a chloride ion 3. Remaining CO2 binds to hemoglobin loosely to form carbaminohemoglobin CO2 can be released in the alveoli & exhaled from the lungs Remaining H binds to HGB to form a weak acid Regulation of pH: 3 ways to respond Maintaining homeostasis Regulation occurs by buffer systems Buffers absorb excess acids and bases Chemical buffer system (purple on diagram) Immediately combines with acids and bases – moment to moment action Prevents large changes in pH, or large acid/base imbalances Bicarbonate = main base in reaction Secondary response = respiratory system Controls elimination of CO2 Rids volatile acids Rids body of volatile acids Third response = kidneys Take longer to work, but are most effective buffer system Rids nonvolatile acids – can eliminate H ions by excreting out of tubular cell And they have the ability to reabsorb base that might be in our filtrate Renal-phosphate and ammonia buffers These buffers combine with H ions in urine filtrate, allowing acid to be excreted from body Phosphate buffering system Diphasic phosphate (HPO4) is found in urine filtrate ¾ is reabsorbed ¼ is used as buffer for H+ in tubular filtrate Combines with secreted H ions from tubular cell Forms monobasic phosphate (H2PO4-) making it lipid insoluble Once it is insoluble, it cannot diffuse back across membrane because lipid insoluble, excreted in urine Deamination (breakdown) of amino acids in renal tubular cells produces NH3 (ammonia) NH 3 secreted into tubular fluid – into urine Combine with H ions in fluid Form ammonium ions NH4+, once formed cannot cross back into the tubular cell Excreted in urine Both of these would allow complete excretion of H ions Tubular cell Urine filtrate ECF Lungs can decrease the amount of carbonic acid by blowing off CO2 & leaving water Respiratory problems involve alteration in CO2 This can reflect increase or decrease in our ventilation Kidneys can absorb bicarbonate and regenerate new bicarbonate from CO2 & water Laboratory data – ABG  pH – 7.35 – 7.45 < 7.35 acidosis > 7.45 alkalosis  CO2 – 35-45mm Hg < 35 alkalosis > 45 acidosis  HCO3 – 22-26mEq/L < 22 acidosis > 26 alkalosis Metabolic acidosis (decreased pH and decreased HCO3-) Causes Production of metabolic acids Acute lactic acidosis Ketoacidosis Decreased renal function Increased bicarbonate losses Diarrhea, fistulas, ileostomies Hypercholermic acidosis Abnormal absorption of Cl- by kidneys Manifestations Neuro – weakness, fatigue CV - peripheral vasodilation GI – N/V, abdominal pain Skin – warm, flushed Compensation Increased respirations Renal Acidic urine (H+ ions) Body getting rid of H+ ions Increased ammonia in urine Occurs as hydrogen is excreted, combines with ammonia to get ammonium Metabolic alkalosis (increased pH and increased bicarbonate/HCO-) Causes Excess base loading Over ingestion of antacids (antacid abusers) IV infusion excess Milk-alkali syndrome Loss of fixed acid Vomiting, GI suction Bulimia Diuretics Fluid depletion with above Manifestations Neuro – confusion, hyperactive reflexes, tetany CV – hypotension, arrhythmias Compensatory R – Hypoventilation Respiratory acidosis (decreased pH and increased PCO2) Causes Increased CO2 production: overuse of drugs, rib injury (no deep breaths), respiratory muscle weakness Acute – rapid rise in CO2 Chronic - COPD Manifestations Neuro – headache, confusion, stupor Skin – warm and flushed Compensation Acid in urine Respiratory alkalosis (increased pH and decreased CO2) Causes Hyperventilation Central stimulation of medullary center of brain Pain Pregnancy Sepsis/febrile states Encephalitis/TBI Mechanical ventilation Hyperventilation syndrome Manifestations S&S Neuro - Lightheadedness, panic, tingling & numbness CV – sweating, palpitations R – dyspnea, air hunger Compensation Alkaline urine (getting rid of bicarbonate ions) GASTRO-INTESTINAL ALTERATIONS Dysphagia (swallowing disorder) Causes Esophageal narrowing (possibly caused by scarring) Decreased salivation Stroke Affects cranial nerves that help coordinate swallowing Trigeminal nerve = chewing Vagus nerve innervates esophagus Glossopharyngeal nerve (9) moves muscles of pharynx Hypoglossal nerve (12) controls tongue Sign & Symptoms Coughing Choking Food sticking sensation in throat or upper chest Achalasia (swallowing disorder) Problem of relaxation of lower esophageal sphincter (LES) When sphincter cannot relax, no food can get in stomach Food stasis and obstruction occurs Can have feelings of dysphagia Might get distended Primary causes: Born without adequate innervation Autoimmune disorders can effect denervation of LES Consequences Inflammation and ulceration Enzymes in saliva help break down food to swallow – these enzymes now in esophagus instead of down in stomach with food Aspiration As with dysphagia; food keeps backing up, greater chance of being aspirated into lungs High risk of esophageal cancer from this Gastroesophageal Reflux (GERD) Persistent reflux upward Contents shoot back up into lower esophagus Causes heartburn (stomach acid reflexing up in lower esophageal area) Causes: Relaxation of lower esophageal sphincter, can happen with high fatty diets (relaxes LES) Chocolate, caffeine, smoking, and alcohol do this as well Decreased salivation and decreases peristalsis contributes to GERD Pregnancy – pressure from fetus can cause heartburn All of this results in mucosal injury Salivary bicarbonate in saliva helps wash away acid Symptoms Heartburn that occurs 30-60 min after meal Can also occur during sleep Laying down – gravity; relaxed LES – easier for reflux to get up into esophagus Belching is common Chest pain MI’s often mistaken for indigestion Hoarse voice if reflux affects vocal cords Can stimulate cough Over time Inflammatory response over time: increased blood flow to area Edema Ulcerations within esophageal tract Fibroblasts / reparative process: constrictures caused from scar tissue Complications Barrett’s esophagus Changes in epithelial lining of esophagus (starts looking like mucosal surface of intestine) Metaplasia – increased risk of cancer when Barrett’s esophagus is developed Acute gastritis refers to transient inflammation of the gastric mucosa, which can be caused by: Diarrhea Food allergies Aspirin Gastric reflux Answer: aspirin (change color) Acute gastritis Acute injury to protective mucosal barrier; can lead to sloughing off of lining of stomach Mucosal barrier prevents gastric secretions from injuring epithelial lining Transient (because it is acute, it only lasts for short periods of time) Causes Aspirin and NSAIDs Affect prostaglandin production (as do corticosteroids) In stomach, prostaglandins help with mucous production Decreased mucous = decreased protection Also have to do with bicarbonate  neutralizes acids Corticosteroids, aspirin, and NSAIDs cut down on stomach’s ability to produce good mucous and bicarbonate  leads to erosions Complaints – depends on cause Vague abdominal discomfort N/V may occur Alcohol affects mucosal lining, causes nausea Hematemesis (bloody vomit) When mucosal lining regenerates, we feel better Self-limiting Food poisoning – bacterial toxins in food Causes havoc 5-6 hours later Chronic autoimmune gastritis can lead to: Pernicious anemia H, pylori infection Weight gain Peptic ulcer disease Answer: pernicious anemia (change color) Chronic gastritis Different from acute because there are no erosions Chronic Autoimmune (Type A) Associated with other autoimmune disorders Slow onset, affects fundus (fundal part of stomach) Antibodies against gastric chief cells, parietal cells & intrinsic factor Body makes antibodies against own cells of stomach Gastric chief cell function is to release pepsinogen that breaks down fats Main problem: parietal cells (they normally secrete HCl which helps break down food) Also responsible for intrinsic factor (vitamin B12 carrier) Causes pernicious anemia Symptoms (similar to those of pernicious anemia) Smooth tongue Numbness/tingling neuropathies Mal-absorptive diarrhea (body cannot absorb nutrients) Chronic Antral (Type B) – non-immune H. Pylori infections Helicobacter pylori gastritis Chronic inflammatory disease that affects antrum & body of stomach (Type B) Gram-negative rods; survive in stomach Colonize mucus secreting epithelial cells The bacteria produce ammonia to buffer acidity and can survive Inflammation Recruits lymphocytes, mediators Causes edema and damage to mucosal lining Symptoms - vary Acute N/V Abdominal pain Chronic Can be asymptomatic until enough of lining is destroyed Constant repair process  fibrous/scarred epithelial lining Risk of cancer increased Peptic ulcers can occur H. Pylori  damages stomach lining Either leads to peptic ulcer OR repair and healing results, but this leads to increased risk of gastric cancer Peptic ulcer disease – ulceration of upper GI tract (stomach and duodenum) Often seen in elderly, alcoholics, and some post-surgical patients Duodenal ulcers common in younger patients Remission & exacerbations (feel pain, goes away, feel pain) Healing scar tissue erodes gastric lining Reparative tissue not as strong as original tissue Areas prone to breakdown Easy re-ulceration Risk Factors H. Pylori (causes 90% peptic ulcers) NSAIDs (aspirin, ibuprofen) Smoking, history of peptic ulcer disease, age Smoking affects reparative process Ulcer classifications Superficial Goes through mucosa but not musculature True Goes through all layers Symptoms: Burning and gnawing cramp-like pain in epigastric region that can radiate along costal margins or to back Pain relieved with food Sudden onset of weakness Thirsty (low circulating volume) Dizzy Cold, moist skin Bleeding: see bloody stool or black tarry stool Vomiting (emesis): caused by partially digested blood Feel full quickly Complications Hemorrhage if it erodes a vessel Perforation Possibly erosion into biliary tract or pancreas Peritonitis occurs when acid in stomach spills into peritoneum (a sterile space) Outlet obstruction Food can’t move downward, patients could vomit indigested food Stress ulcer Ulcer derived from major physiologic stress Curling’s ulcer = stress ulcer affecting part of stomach or duodenum High risk – common in hospital setting Major surgical procedures, trauma, large burns Liver failure (severe) Sepsis All impair blood flow in some way Ischemia to stomach lining: starvation of blood flow can cause ulcer Painless upper GI tract bleeding But CAN be painful and thirsty Patients with Crohn’s disease may experience whichof the following complications? Chronic constipation Excessive weight gain Fistula formation Difficulty swallowing Answer: fistula formation (change color) Crohn’s disease and ulcerative colitis (comparison) Both disorders: Are inflammatory – exacerbations and remissions Lifelong inflammatory response causes tissue damage in GI tract Diarrhea, fecal urgency, weight loss Crohn’s disease affects ANY AREA of GI tract and all layers of bowel, but affects submucosal the greatest (see second picture) Skip lesions: hallmark of Crohn’s disease (Normal bowel, diseased bowel, normal bowel, diseased bowel, etc) Ulcerative colitis: Starts at rectum and works its way up ONLY affects colon (“colitis”) Primarily affects mucosal layer, not submucosal as in Crohn’s disease Crohn’s Disease Cobblestone appearance to GI tract caused by inflammation of submucosal layer Crevices between villi (all submucosal; pushing up) Granulomatous inflammatory response Starts in submucosal later and this is where fibrotic changes occur Risk Factors Women 20-30 years Family history Jewish ethnicity Tobacco use Urban residency (environmental factor) Lesions Granulomatous & demarcated Skip lesions Normal and abnormal bowel Exacerbations & remissions Inflammation narrows lumen of GI tract Overtime bowel wall thickens & becomes inflexible Gradual narrowing prone to obstruction Complications Patients can develop abscesses and fistulas WBCs, pus from inflammation Signs and symptoms (related to location of diseased part of bowel) Intermittent diarrhea Colicky pain (mostly in RLQ) Skin around anus prone to ulcerations Malaise and fatigue Low-grade fever Fluid & electrolyte imbalances Steatorrhea Fatty diarrhea, can cause dehydration Nutritional deficiencies Losing absorptive process of bowel If ileum involved, this is where intrinsic factor crosses over Patients at risk for vitamin B12 deficiency Patients at risk for hypocalcemia and folic acid deficiency Weight loss Nutrients not being absorbed, diarrhea Ulcerative colitis is characterized by: Gastric ulcers Pseudopolyps Skip lesions Steatorrhea Answer: pseudopolyps (change color) Ulcerative colitis Begins in rectum and works proximally Chronic inflammation  ulceration Risk Factors Younger population, 20-40 years Family history, Jewish ancestry, northern European descent Lesions Form in crypts of Lieberkuhn in mucosal layer base (top layer of bowel) Mild - hyperemic & edematous  dark red & velvety bowel Hyperemia (lots of blood flow) gives velvety looking bowel Severe - mucosal hemorrhages  abscess  necrosis & ulcerate Pseudopolyp formation Thickening of bowel wall from inflammatory response Diarrhea can be more severe in this form; can last longer Exacerbations and remissions Relapsing disorder Complications At risk for colon cancer Symptoms Diarrhea Days to months Contain blood & mucus From ulceration of mucosal layer Mild cramping Related to destruction of mucosal layer Anorexia Weakness Weight loss Anemia (severe) Dehydration (severe) Fever (severe) Which of the following is a factor in the development of diverticulitis? Alcohol consumption Diet low in fiber Recent abdominal surgery H. Pylori infection Answer: diet low in fiber (change color) Terminology of diverticular disease Diverticula – saclike outpouchings of mucosa through muscle layers of colon Diverticulosis – diverticula without inflammation Diverticulitis – inflammation of diverticula or gross perforation of diverticula Diverticulosis and diverticulitis Affects older population > 60 Most common site of diverticular disease: left/sigmoid colon Has to do with diet low in fiber, decreased physical activity, poor bowel habits Lack of fiber causes it because it helps regulate bowel movements Goal: 1 formed bowel per day – water and fiber keep this regular Diverticula form in weak points of bowel wall They are herniations between muscle layers Occur due to increased pressure within bowel Diverticulosis Ill-defined lower abdominal discomfort Change in bowel habits Diarrhea, constipation Bloating & flatulence Diverticulitis Pain & tenderness in LLQ from inflammation N/V Fever, elevated WBC from inflammation Complications Weakens bowel wall, outpouchings of bowel can become inflamed and weakened then perforate Perforation of bowel – spilling stool into abdominal cavity Enlarged inflammatory response causes obstruction along with edema of bowel Lots of pus that can become necrotic and lead to perforation or abscess formation Acute intestinal obstruction: partial or complete blockage of bowel Mechanical: impaired flow of chyme (broken-down food traveling through GI tract) Another cause: Surgery in abdominal cavity – after surgery the tissues can become sticky and stick together Non-mechanical: motility issue Very common after GI surgeries because handling of bowel Bowel does not like to be touched and moved around They “get angry and fall asleep” Other non-mechanical problems have to do with opioids and anesthetics: significantly slows down motility Inflammatory reactions: peritonitis affects motility Any kind of neuromuscular impairment – spinal cord injury – more prone to bowel obstructions (cannot ambulate) Ambulation does a lot to keep us regular Hypokalemia: can cause atony (a lack of muscle movement) of GI tract Mechanical acute intestinal obstruction: impaired flow Intussusception: telescoping of bowel (one part of bowel engulfs another part); we see this in children Cause could be a mass within area of bowel – creates traction Volvulus: a twisting of bowel Mesentery Hernia: in picture of this male, bowel dropped down inguinal canal They can be femoral, inguinal, or umbilical Simple obstruction: no interruption in blood flow Strangled obstruction: lack of blood supply (i.e. in volvulus) Losing blood flow: bowel dies and becomes necrotic Hernia (bowel pushes out in muscle layer) Reducible (most common) Can be pushed back into place Incarcerated: non-reducible Lose ability to push it back in, often seen in umbilical hernias Strangulated: give us the most problems because there is a lack of blood flow Intense pain, vomiting, swelling Surgery required due to lack of blood flow Intestinal obstruction Obstruction (narrowing of bowel; fluid, electrolytes, food not getting down) Distension (squeezes areas)  venous return  bowel wall edema Lose ability to absorb H2O & electrolytes (collection of fluid) Increased distension Necrosis Perforation *Some reasons we become distended because we swallowing a lot of air during the day Combination of fluid, food, and air Air is poorly absorbed, gas accumulation occurs In GI tract, we have good bacteria to help breakdown food A translocation can happen in intestinal obstruction in which we lose the good bacteria that get into bloodstream (patients can become sick) Severe obstructions can cause strangulations – can lead to necrosis (& bowel wall can break – GI content ends up in abdomen) Dehydration due to not absorbing and vomiting S&S Bowel sounds Hyper-peristalsis because body trying to push past obstruction If complete obstruction, can hear tympany when percussing from all the air accumulating Pain Mechanical Body trying to force past obstruction: when bowels contract, spasm-like pain Intermittent/colicky (pain leaves when bowel relaxes) Paralytic (non-mechanical) Constant pain without bowel sounds Motility issue; often will not hear bowel sounds Strangulation Lack of blood flow Starts out as mechanical (spasm like) pain  steady, severe pain Distended abdomen Vomiting Fluid cannot get past obstruction, has to go somewhere Dehydration Electrolyte depletion Hypokalemia = biggest depletion from obstruction Bowel movements Partial obstruction can cause diarrhea or constipation Some stool still getting by Complete obstruction - constipation Peritonitis Inflammation of serous membranes within abdomen: rebound tenderness felt Viscera covers abdominal organs – if viscera is inflamed it’s very painful Caused by bacterial invasion of peritoneum Any rupture within bowel can cause peritonitis Abdominal wounds Pelvic inflammatory disease Intense pain aggravated with movement – patients don’t want to move or even take a deep breath Distended abdomen (see picture) Guarding their belly They may vomit No bowel sounds heard “itis” – could be a fever and elevated WBCs Gallbladder disease Bile needed for digestion of fats and absorption of fat-soluble vitamins Cholelithiasis (gall stones) Cholecystitis – stone leaves and gets into duct of bladder Might see impaired digestion of fats Types Cholesterol stones Pigmented stones Risk factors Obesity (high dietary intake of cholesterol) Middle-aged Female or using contraceptives American Indian ancestry S & S Asymptomatic OR Might have mild fever (“itis – inflammation) Nausea and vomiting Complications When stone gets lodged in a duct – inflammation occurs behind obstruction Spasm-like/colicky pain results Can be intermittent or steady depending on size Can cause pancreatitis if it affects output of pancreas (obstructs that part of cystic duct) Gangrene of gall bladder from lack of blood flow Development of abscesses Perforations If stone is severe or there are multiple stones and it affects bile release – some patients could develop jaundice if obstruction occurs in common bile duct What can also happen: if people have gall bladder attacks and then pain ceases, patients might have intolerance to fatty foods Fatty stools from impaired bile/impaired digestion of fat Super-saturation of cholesterol in bile  crystal formation  microstones and increased crystals  macrostones  cholelithiasis OR cholecystitis Acute pancreatitis Auto-digestion of pancreatic tissue (enzymes are eating pancreas) causing inflammation Causes Gallstone blocking duct Sign & Symptoms Cardinal sign = abdominal pain that can radiate to flank and back One of most painful things people can endure Unrelieved by antacids Edema from inflammation (capillary permeability) N/V (vomiting does not provide relief) Complications Fluid collection Diagnosis of pancreatitis: amylase and lipase lab studies Exocrine/enzyme functions of pancreas help breakdown food products Alcoholics – stimulates pancreatic secretions – they back up and auto digest Inflammatory response: fever, tachycardia (so much capillary permeability that patients also become hypotensive) Erosion of vessels of pancreas; flank = gray Chronic pancreatitis Causes longstanding obstruction of pancreatic duct Lose endocrine and exocrine function once pancreas becomes fibrotic (progressive destruction with fibrotic replacement) Losing endocrine function causes hyperglycemia Losing exocrine function causes mal-absorptive problems, fatty stools Causes Alcohol abuse (number 1 cause) Sign & Symptoms Pain, nausea, vomiting HEPATIC ALTERATIONS Liver Facts Largest internal organ Approximately 25% of the cardiac output feeds the liver Performs more that 400 functions All blood goes to liver before going back to heart Filters out bacteria and toxins Sinusoids Blood supply from portal vein & hepatic artery 2 types of cells Endothelial cells Line capillaries Reticuloendothelial (Kupffer) The liver’s own macrophages = Kupffer cells Within the sinusoids, there is intimate contact with each hepatocyte When liver becomes diseased and fibrotic, these become bigger and impinge on blood flow/biliary flow in the liver Bile canaliculi Lie between hepatocytes Functioning cells of the liver Drains bile to larger ducts for removal Check out Table 30-1 for altered function Liver used for Storage, Detoxification, Phagocytic Metabolic Breakdown of picture: (shows certain dietary functions) Glucose metabolism Stores glucose as glycogen Synthesizes glucose from AA & other substrates Converts excess CHO to triglycerides (stored in adipose) Lipid metabolism Oxidation of free fatty acids to ketoacids Synthesis of cholesterol, phospholipids & lipoproteins Formation of triglycerides from CHO & Proteins Protein metabolism
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